4/19/2019 Intestinal Perforation: Background, Anatomy, Pathophysiology

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Intestinal Perforation
Updated: Nov 28, 2018
Author: Samy A Azer, MD, PhD, MPH; Chief Editor: John Geibel, MD, DSc, MSc, AGAF more...

OVERVIEW

Background
Upper-bowel perforation can be described as either free or contained. Free perforation occurs when
bowel contents spill freely into the abdominal cavity, causing diffuse peritonitis (eg, duodenal or gastric
perforation). Contained perforation occurs when a full-thickness hole is created by an ulcer, but free
spillage is prevented because contiguous organs wall off the area (as occurs, for example, when a
duodenal ulcer penetrates into the pancreas).

Lower-bowel perforation (eg, in patients with acute diverticulitis or acute appendicitis) results in free
intraperitoneal contamination.

Lau and Leow have indicated that perforated peptic ulcer was clinically recognized by 1799, but the
first successful surgical management of gastric ulcer was by Ludwig Heusner in Germany in 1892. In
1894, Henry Percy Dean from London was the first surgeon to report successful repair of a perforated
duodenal ulcer. [1]

Partial gastrectomy, although performed for perforated gastric ulcer as early as 1892, did not become
a popular treatment until the 1940s. This was carried out as a result of the perceived high recurrence
rate of ulcer symptoms after simple repair. The physiologic effects of truncal vagotomy on acid
secretion had been known since the early 19th century, and this approach was introduced to the
treatment of chronic duodenal ulcer in the 1940s.

The next development in the management of peptic ulcer disease was the introduction of high
selective vagotomy in the late 1960s. However, neither of these approaches proved to be useful, and
several postoperative complications, including high rates of ulcer recurrence, have limited their use.
Currently, in patients with gastric perforation, simple closure of perforated ulcers is more commonly
performed than is gastric resection. [2]

During World War I, the mortality following isolated injuries of the small intestine and colon was
approximately 66% and 59%, respectively. The possible reasons for the high mortality and morbidity
rates at that time may have been related to the following factors:

Knowledge in the area of bowel injuries and the pathophysiologic changes triggered by such
injuries was inadequate
Clinical skills and diagnostic techniques that allow early detection of such injuries were lacking
Intravenous saline solutions or blood transfusions were not used in the management of
hypovolemia and hemodynamic changes of these patients
No antibiotics were available
Laparotomy was not recommended in abdominal injuries
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4/19/2019 Intestinal Perforation: Background, Anatomy, Pathophysiology

The technical maneuvers to assess bowel injuries and to mobilize ascending and descending
colon were generally not recommended

During the early years of World War II, Ogilvie, a leading surgeon in the British Army, recommended
colostomy for management of all colonic injuries. This notion was supported by a publication from the
office of the Surgeon General of the United States. However, the data presented in Ogilvie's series
were not convincing. He reported a mortality rate of 53% for colonic injuries treated with colostomy, a
rate similar to that observed during World War I.

According to Ogilvie, colostomy apparently failed to improve the mortality rate in World War II because
primary repairs were used to treat less-severe injuries during World War I. Many patients in World War
I were treated expectantly and were not included in the mortality data. On the other hand, Ogilvie's
data included all patients with bowel injuries. These apparent differences in the methodology used
convinced surgeons to continue using colostomies in such injuries after World War II.

Several reports clearly indicated that surgeons used colostomy during the Korean and Vietnam wars,
particularly in the management of left colonic injuries. However, in civilian injuries, it has been reported
that primary repair can be successfully used. By the end of 1980s, primary repair was considered to
the management strategy of choice, and it has replaced the use of colostomies in the treatment of
civilian patients in most hospitals in the United States, the United Kingdom, Europe, and Australia. At
present, primary repairs are widely used for such bowel injuries.

Anatomy
The peritoneal cavity is lined with a single layer of mesothelial cells, connective tissue (including
collagen), elastic tissues, macrophages, and fat cells. The parietal peritoneum covers the abdominal
cavity (ie, abdominal wall, diaphragm, pelvis); the visceral peritoneum covers all of the intra-abdominal
viscera, forming a cavity that is completely enclosed except at the open ends of the fallopian tubes.

The peritoneal cavity is divided by the transverse mesocolon. The greater omentum extends from the
transverse mesocolon and from the lower pole of the stomach to line the lower peritoneal cavity. The
pancreas, duodenum, and ascending and descending colon, are located in the anterior retroperitoneal
space; the kidneys, ureters, and adrenal glands are found in the posterior retroperitoneal space. The
liver, stomach, gallbladder, spleen, jejunum, ileum, transverse colon, sigmoid colon, cecum, and
appendix are found within the peritoneal cavity.

A small amount of fluid sufficient to allow movement of organs is usually present in the peritoneal
space. This fluid is normally serous (protein content of < 30 g/L, < 300 WBCs/µL). In the presence of
infection, the amount of this fluid increases, its protein content climbs to more than 30 g/L, and the
white blood cell (WBC) count increases to more than 500/µL; in other words, the fluid becomes an
exudate.

Pathophysiology
Normally, the stomach is relatively free of bacteria and other microorganisms because of its high
intraluminal acidity. Most persons who experience abdominal trauma have normal gastric functions

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4/19/2019 Intestinal Perforation: Background, Anatomy, Pathophysiology

and are not at risk of bacterial contamination following gastric perforation. However, those who have a
preexisting gastric problem are at risk of peritoneal contamination with gastric perforation.

Leakage of acidic gastric juice into the peritoneal cavity often results in profound chemical peritonitis.
If the leakage is not closed and food particles reach the peritoneal cavity, chemical peritonitis is
succeeded by gradual development of bacterial peritonitis. Patients may be free of symptoms for
several hours between the initial chemical peritonitis and the later occurrence of bacterial peritonitis.

The microbiology of the small bowel changes from its proximal to its distal part. Few bacteria populate
the proximal part of the small bowel, whereas the distal part of the small bowel (the jejunum and
ileum) contains aerobic organisms (eg, Escherichia coli) and a higher percentage of anaerobic
organisms (eg, Bacteroides fragilis). Thus, the likelihood of intra-abdominal or wound infection is
increased with perforation of the distal bowel.

The presence of bacteria in the peritoneal cavity stimulates an influx of acute inflammatory cells. The
omentum and viscera tend to localize the site of inflammation, producing a phlegmon. (This usually
occurs in perforation of the large bowel.) The resulting hypoxia in the area facilitates growth of
anaerobes and produces impairment of bactericidal activity of granulocytes, which leads to increased
phagocytic activity of granulocytes, degradation of cells, hypertonicity of fluid forming the abscess,
osmotic effects, shift of more fluids into the abscess area, and enlargement of the abdominal abscess.
If untreated, bacteremia, generalized sepsis, multiorgan failure, and shock may occur.

Etiology
Causes of intestinal perforation include the following:

Penetrating injury to the lower chest or abdomen (eg, knife injuries) - In cases of penetrating
trauma, the small bowel is the most commonly injured intra-abdominal viscus, because it is
coiled in the abdomen and occupies most of the area of the peritoneal cavity; in addition, the
small bowel is attached to a mesentery and is highly mobile
Blunt abdominal trauma to the stomach - Such injuries are more common in children than they
are in adults and include vehicle-related trauma, bicycle handlebar injuries, and seatbelt
syndrome
Ingestion of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), [3] and steroids - Intestinal
perforation from such causes is particularly observed in elderly patients; prescribing NSAIDs to
patients with diverticular disease carries an increased risk of colonic perforation
Presence of a predisposing condition - Predisposing conditions include peptic ulcer disease,
acute appendicitis, acute diverticulitis, and inflamed Meckel diverticulum; indeed, acute
appendicitis is still one of the common causes of bowel perforation in elderly patients and is
associated with relatively poor outcomes [4]
Bowel injuries associated with endoscopy - Injuries can occur with endoscopic retrograde
cholangiopancreatography (ERCP) and colonoscopy [5, 6, 7, 8]
Endoscopic biliary stent - Dislocation and migration of biliary stents to the intestine may cause
bowel perforation [9]
Intestinal puncture as a complication of laparoscopy - Factors that may predispose patients to
this complication are obesity, pregnancy, acute and chronic bowel inflammation, and bowel
obstruction
Bacterial infections - Bacterial infections (eg, typhoid fever) may be complicated by intestinal
perforation in about 5% of patients; perforation in these patients may unexpectedly occur after
their condition has started to improve
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Inflammatory bowel disease - Bowel perforation may occur in patients with acute ulcerative
colitis, and perforation of the terminal ileum may occur in patients with Crohn disease (CD); the
CD-associated gene SLCO3A1 has been shown to mediate inflammatory processes in intestinal
epithelial cells and thereby result in a higher incidence of bowel perforation in CD patients [10]
Perforation secondary to intestinal ischemia (eg, ischemic colitis)
Bowel perforation by intra-abdominal malignancy, lymphoma, or metastatic renal carcinoma -
Even benign tumours, such as desmoid tumours (eg, those originating from the fibrous tissues of
the mesentery), may cause bowel perforation [11]
Radiotherapy of cervical carcinoma and other intra-abdominal malignancies - This may be
associated with late complications, including bowel obstruction and bowel perforation [12]
Necrotizing vasculitis - Wegener granulomatosis affecting the viscera, though uncommon, may
cause bowel ulcerations and perforations [13]
Kidney transplant - After a kidney transplant, gastrointestinal (GI) perforations may occur as a
complication; in these cases, the perforation is usually related to the use of high doses of
immunosuppressive medications, a treatment employed in the early postoperative period and in
the management of acute rejection episodes [14]
Ingestion of caustic substances - Accidental or intentional ingestion of caustic substances may
result in acute intestinal perforation and peritonitis; delayed perforation may occur up to 4 days
after acid exposure
Foreign bodies (eg, toothpicks) - These may cause perforation of the esophagus, stomach, or
small intestine, with intra-abdominal infection, peritonitis, and sepsis

Epidemiology
In children, small-bowel injuries following blunt abdominal trauma are infrequent, with an incidence of
1-7%. Evidence shows, however, that the incidence of these injuries is increasing.

In adults, perforations of peptic ulcer disease were a common cause of morbidity and mortality with
acute abdomen until the latter half of the 20th century. The rate has fallen in parallel with the general
decline in the prevalence of peptic ulcer disease. Duodenal ulcer perforations are 2-3 times more
common than are gastric ulcer perforations. About a third of gastric perforations are due to gastric
carcinoma.

Approximately 10-15% of patients with acute diverticulitis develop free perforation. Although most
episodes of perforated diverticulum are confined to the peridiverticular region or pelvis, patients
occasionally present with signs of generalized peritonitis. The overall mortality is relatively high (~20-
40%), largely because of complications, such as septic shock and multiorgan failure.

In elderly patients, acute appendicitis has a mortality of 35% and a morbidity of 50%. A major
contributing factor to morbidity and mortality in these patients is the presence of 1 or more severe
medical conditions coexisting with, but predating, the appendicitis.

Endoscopy-associated bowel injuries are not a common cause of perforation. For example,
perforations related to ERCP occur in about 1% of patients. [5]

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Prognosis
Outcome is improved with early diagnosis and treatment. The following factors increase the risk of
death:

Advanced age
Presence of preexisting underlying disease
Malnutrition
The nature of the primary cause of bowel perforation
Appearance of complications

Clinical Presentation

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